AFIP Wednesday Slide Conference - No. 17
January 20, 1999

Conference Moderator:
Dr. Jerry L. Quance, Diplomate, ACVP
Maryland Department of Agriculture
Animal Health Laboratory
Frederick, MD 21702.
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Case I - UCD 2 (AFIP 2648198)

Signalment: Thirteen-year-old, male, gelded, quarter horse.
History: The horse was presented with a one week history of weight loss, drooling, and progressive central nervous system signs that included a "worried" look, incoordination with leaning to the left, staggering and disorientation, violent movements to maintain balance, and episodes of falling down with eventual recumbency and thrashing movements. In addition, there was absence of menace response and palpebral reflexes, and suspected loss of vision on the right side. The horse had been vaccinated for rabies and tetanus four months previous to the onset of clinical signs. He was treated with flunixin meglumine, dexamethasone, and antibiotics, but he continued to decline rapidly over the following two days and died.
Gross Pathology: Findings included skin lacerations and contusions from self-trauma and moderate muscle atrophy. The meninges along the ventral brain stem were congested, and multifocal, randomly distributed, 4-6 millimeter, brown-gray foci were present in the ventral midbrain.
Laboratory Results:
1. Clinical chemistry and hematological abnormalities included elevated direct/indirect bilirubin (0.6/3.6) and slight neutrophilia with marked lymphopenia.
2. Rabies fluorescent antibody was negative.
3. Sections of brain stem were immunohistochemically positive for Listeria monocytogenes.
4. Listeria monocytogenes was isolated from sections of brain stem.
Contributor's Diagnosis and Comments: Brain stem: Encephalitis, multifocal, suppurative, acute, severe.
The brain stem contains extensive, multifocal to coalescing areas of inflammation with multiple microabscesses and variably thick cuffs of perivascular inflammation. Inflammation extends into the medulla and cervical spinal cord. Inflammatory infiltrates are composed of predominately degenerate neutrophils admixed with fewer macrophages and small amounts of eosinophilic necrotic tissue debris. Perivascular inflammation contains variable numbers of neutrophils, lymphocytes, and macrophages. In some vessels, inflammatory cells appear to be present within and expand the vascular walls. Mild multifocal hemorrhage is associated with the inflammation.
The histopathology is compatible with listeriosis, and this was confirmed both by immunohistochemistry on sections of brain and isolation of Listeria monocytogenes from frozen brain stem. Differential diagnosis considered for the gross lesions in the midbrain was yellow star thistle poisoning, but the histology consists of coalescing microabscesses, which is more consistent with listeriosis. A search of the California Veterinary Diagnostic Laboratory Service case files found only one other diagnosed case of equine listeriosis, a case of Listeria encephalitis and septicemia in a five-week-old foal.
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Case 17-1. Brainstem. Vessels are congested and cuffed by inflammatory cells. There is multifocal perivascular hemorrhage. High magnification reveals that perivascular inflammatory cells are predominantly viable & occassionally degenerate neutrophils with variable numbers of macrophages and lymphocytes.
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Case 17-1. Brainstem. Bacilli and coccobacilli are found with B&B staining.
AFIP Diagnosis: Brain stem: Encephalitis, subacute, multifocal, moderate, with microabscesses, hemorrhage, and mild meningitis, quarter horse, equine.
Conference Note: Listeriosis is caused by a Gram-positive, facultative anaerobic bacillus that is ubiquitous in the environment and able to resist harsh environmental conditions. Organisms can survive in dried media for several months, remain viable in moist soil for up to ten years, resist high temperature pasteurization within leukocytes, and can grow at refrigeration temperature. Until recently, Listeria monocytogenes was the only member of the genus, but Listeria ivanovii, L. innocua, L. welshimeri, and L. seeligeri are now separately recognized. Clinical infections are most commonly caused by L. monocytogenes, though L. ivanovii is also pathogenic and has been associated with abortion in ruminants. The other species are considered nonpathogenic.
Listeriosis is a sporadic disease of several animal species and humans, but is most economically important in ruminants. Infection with L. monocytogenes is associated with a triad of clinicopathologic syndromes: most often it causes in encephalitis in adult animals; it occasionally causes placentitis and abortion in pregnant animals; and it is an infrequent cause of septicemia in neonates. Listeriosis is one of the most common causes of meningitis in humans and nonhuman primates. Listeric septicemia often results in multifocal hepatic and splenic necrosis, in addition to central nervous system lesions; neonates generally become infected in utero. Sporadic cases of listeric septicemia also occur in domestic fowl, resulting in splenomegaly, hepatic and myocardial necrosis, and occasional encephalitis. Keratoconjunctivitis and iritis caused by L. monocytogenes has been reported to occasionally occur in silage fed cattle and sheep; the condition is usually unilateral and frequently occurs in winter.
In encephalitic listeriosis, clinical signs reflect lesions in the brain stem and include dullness, torticollis, circling, unilateral facial paralysis, and drooling due to pharyngeal paralysis. Death in sheep and goats may occur in two to three days, while cattle may survive longer periods. Gross lesions are rarely identified in the brain, but occasionally the meninges may be thickened by green gelatinous material, and soft, gray-brown malacic areas may be present in the brain stem. Characteristic histopathologic findings in the central nervous system occur most often in the brain stem and less frequently in the cerebellum and cervical spinal cord. Microscopic lesions consist of microabscesses in the neuropil, heavy perivascular infiltrates of lymphocytes, histiocytes, and occasional neutrophils, acute vasculitis with fibrin exudation, and meningitis. The ependyma and choroid plexus are rarely affected.
Several virulence factors for L. monocytogenes have recently been identified and defined. The organism is capable of surviving and multiplying within macrophages. The bacterium enters the host cell, escapes destruction in the phagosome, multiplies within the cytoplasm, and spreads to other cells. The ability of the organism to lyse the phagosomal membrane through secretion of hemolysin and listeriolysin and escape into the cytoplasm is a key virulence factor. Another virulence factor is the ability of the organism to move within the cytoplasm; this is mediated by a bacterial surface protein that causes polymerization of host cell actin filaments and propels the organism into neighboring cells. Several other virulence factors are discussed in a recent review article of listeriosis cited in the references. While virulence factors have been well-characterized, the exact route of infection in the encephalitic form of the disease remains to be determined. Experimental studies have not conclusively determined the pathogenesis of listeric encephalitis, and hematogenous routes as well as centripetal passage of bacteria by way of cranial nerves remain possible mechanisms of central nervous system infection.
Contributor: California Veterinary Diagnostic Laboratory Services, School of Veterinary Medicine, Univ. of California Davis, PO Box 1770, Davis, CA 95617.
1. Marco A, et al.: Immunocytochemical detection of Listeria monocytogenes in tissue with the peroxidase-antiperoxidase technique. Vet Pathol 25:385-387, 1988.
2. Weinstock D, Horton SB, Rowland PH: Rapid diagnosis of Listeria monocytogenes by immunohistochemistry in formalin-fixed brain tissue. Vet Pathol 32:193-195, 1995.
3. Wallace S, Hathcock T: Listeria monocytogenes septicemia in a foal. J Amer Vet Med Assoc 207:1325-1326.
4. Low JC, Donachie W: A review of Listeria monocytogenes and listeriosis. The Veterinary Journal 153:9-29, 1997.

Case II - 1953-98 (AFIP 2643248)

Signalment: One-year-old, male, breed unspecified, cat.
History: The cat presented with generalized icterus following castration. The animal bled profusely after castration and developed an atonic bladder.
Gross Pathology: A limited autopsy was performed by the submitting veterinarian. The urinary bladder was described as "inflamed". The kidney and liver were diffusely mottled.
Laboratory Results: None available.
Contributor's Diagnoses and Comments:
1. Urocystitis, necro-ulcerative, pyogranulomatous, transmural, diffuse, due to invasive Candida albicans infection.
2. Tubulointerstitial nephritis, granulomatous, multifocal with intralesional yeast and pseudohyphae of Candida albicans.
Pathologic alterations are limited to the urinary system. The kidneys are bilaterally involved. Brain, spinal cord, and thoracic organs are not available for histopathologic examination. Ascending infection via the ureter is the most likely source of dissemination to the kidney, yet inflammation in the renal pelvis is minimal. Clinically, feline candidiasis is generally associated with immunosuppression. Panleukopenia virus, feline immunodeficiency virus, and feline leukemia virus status in this cat are unknown. Information about emperic treatment, such as antibiotic or glucocorticoid therapy, the presence of an indwelling transurethral catheter, and aciduria may substantiate an immunosuppressive state and help to differentiate acquired predisposing risk factors from inate immunodeficiency conditions and underlying viral infections. Amelioration of risk factors has been associated with spontaneous resolution of funguria in cats. Alkalization of urine and administration of antifungal chemotherapy are needed to control disease.
Production of adhesins, proteases, and capsules contributes to the virulence of fungal infections such as Aspergillus fumigatus, Candida albicans, and Cryptococcus neoformans. In mice, there is evidence of two independent host genes influencing the severity of tissue damage and susceptibility to pyelonephritis in the murine model of systemic candidiasis. It has been shown that host defenses against candidiasis are impaired in intracellular adhesion molecule-1 deficient mice due to impaired neutrophil migration, impaired phagocyte activation, or both.
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Case 17-2. Urinary bladder. Hemorrhage, thrombosis and inflammatory cells replace urothelium and infiltrate underlying smooth muscle. Vessel walls are multifocally replaced by necrotic debris, neutrophils, macrophages and fungal hyphae. Some vessels contain fibrin thrombi.
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Case 17-2. Kidney. Multifocally, tubular epithelium is necrotic and replaced by abundant fungal hypha and pseudohyphae admixed with neutrophils and fewer macrophages. PAS staining illustrates the branching nature of hyphae and the segmentation of pseudohyphae.
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Case 17-2. Kidney. Scattered venous thrombosis is accompanied by pyogranulomatous inflammation replacing vascular walls and extending into the interstitium.
AFIP Diagnoses:
1. Urinary bladder: Cystitis, ulcerative, pyogranulomatous, diffuse, severe, with necrotizing vasculitis, and many hyphae, pseudohyphae, and yeasts, breed unspecified, feline.
2. Kidney: Nephritis, tubulo-interstitial, pyogranulomatous, multifocal, moderate, with vasculitis, fibrin thrombi, and few yeasts.
Conference Note: The mucosa of the urinary bladder is diffusely ulcerated and replaced by a coagulum of hemorrhage, fibrin, edema, high numbers of viable and degenerate neutrophils and macrophages, fewer lymphocytes, and many yeasts. Similar inflammatory cells and yeasts transmurally infiltrate and expand the remainder of the urinary bladder, and there is extensive necrosis of smooth muscle and vessels. Histochemical stains submitted by the contributor, including the Grocott's methenamine silver method counterstained with hematoxylin and eosin and the periodic acid-Schiff reaction, demonstrate many fungal pseudohyphae, septate hyphae, and blastoconidia. A few fungal structures are found within degenerate and necrotic vessels. Morphologically, pseudohyphae are seen as chains of yeastlike cells which remain attached end to end and have prominent constrictions at points of attachment. True hyphae are tubular and have parallel cell walls with no constrictions. Blastoconidia are thick-walled, spherical structures which measure between 8 to 12mm in diameter.
Multifocally, the interstitium of the renal cortex is infiltrated and expanded by moderate numbers of viable and degenerate neutrophils and macrophages, and fewer lymphocytes and plasma cells. Inflammatory infiltrates are oriented around both cortical tubules and vessels; inflammatory cells often infiltrate and expand vessel walls and disrupt the endothelium. Significantly fewer inflammatory cells infiltrate the renal medulla. Examination of special stains reveals radially oriented hyphae and pseudohyphae that fill and disrupt a few subcapsular tubules. Focally, one or two medullary tubules also contain a few fungal hyphae. Organisms were not found within inflamed vessels.
Like the contributor, participants found it difficult to determine the route of fungal dissemination to the kidney. The presence of yeasts within renal tubules, albeit infrequent, suggests an ascending route of renal infection. Hematogenous dissemination of fungi to the kidney was considered by participants due to the vascular lesions and inflammatory cells surrounding vessels, although yeasts were not found within vessel walls or lumens. Additionally, participants considered concurrent infection with the noneffusive form of feline infectious peritonitis (FIP) virus as the cause of pyogranulomatous inflammation multifocally surrounding and disrupting renal cortical vessels. The contributor discusses the potential for underlying viral infection in this cat, and notes several prediposing factors associated with feline candidiasis including various causes of immunosuppression. The history, signalment, and description of clinical signs provided by the contributor are also suggestive of FIP. Approximately 50% of cats with FIP are young (2 years or less), and may have a history of recent stress. In the noneffusive form, multiple organ systems may be affected, including the liver, and hepatic insufficiency and icterus may occur. The stress of castration may have triggered the development of both renal candidiasis and noneffusive FIP. It is unfortunate that other tissues were not available for microscopic examination.
Contributor: C. E. Kord Animal Disease Diagnostic Laboratory, P.O. Box 40627, Melrose Station, Nashville, TN 37204.
1. Davies C, Troy GC: Deep mycotic infections in cats. J Amer Anim Hosp Assoc 32:380-391, 1996.
2. Ashman RB, et al.: Evidence that two independent host genes influence the severity of tissue damage and susceptibility to acute pyelonephritis in murine systemic candidiasis. Microbial Pathogenesis 22:187-192, 1997.
3. Lulich JB, Osborne CA: Fungal infections of the feline lower urinary tract. Vet Clin N Amer Small Anim Pract 26:309-315, 1996.
4. Davis SL, et al.: Host defenses against host disseminated candidiasis are impaired in intracellular adhesion molecule-1 deficient mice. J Infect Dis 174: 435.
5. Jones TC, Hunt RD, King NW: Diseases caused by viruses. In: Veterinary Pathology, 6th ed., pp. 352-353, Williams and Wilkins, Baltimore, 1997.
6. Greene CE, Chandler FW: Candidiasis, torulopsosis, and rhodotorulosis. In: Infectious Diseases of the Dog and Cat, Greene CE, ed., 2nd ed., pp. 414-417, WB Saunders Co., Philadelphia, 1998.

Case III - 17680-98 (AFIP 2641600)

Signalment: Six-week-old, crossbred, domestic pig.

History: Three to four weeks post-weaning, pigs became unthrifty. Clinical signs included fever and dyspnea.
Gross Pathology: There were moderate numbers of loose fibrin strands in the peritoneal and thoracic cavities. Lungs were diffusely dark red and contained dark purple accentuated lobules. The liver was enlarged, and a marked amount of blood exuded from its cut surface. The contents of the small and large intestines had a semifluid consistency.
Laboratory Results: Salmonella cholerasuis var. kunzendorf was isolated from a composite of lung and liver.
Contributor's Diagnosis and Comments: Severe subacute multifocal, histiocytic and neutrophilic hepatitis with necrosis, Salmonella cholerasuis var. kunzendorf.
The liver is characterized by severe multifocal hepatocellular necrosis. The necrotic foci vary in appearance. Many necrotic foci are characterized by coagulation necrosis with hemorrhage, while other foci contain histiocytes and degenerate neutrophils or a mixed mononuclear cell infiltrate consisting of histiocytes and occasional lymphocytes and plasma cells. Fibrin thrombi can be seen in periportal veins and in sinusoids. Moderate to high numbers of mixed mononuclear inflammatory cells infiltrate periportal areas.
The lesions that occurred are caused by endothelial damage by endotoxin and localization of organisms within affected tissues. Salmonellosis is a major concern to veterinarians and pork producers as a cause of septicemia and diarrhea in pigs. Some species of salmonella are a major concern as food-borne pathogens for humans.
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Case 17-3. Liver. Multifocally there are small foci of necrosis containing cell debris, and variable numbers of neutrophils and macrophages (paratyphoid nodules).
AFIP Diagnosis: Liver: Hepatitis, random, necrotizing, acute, multifocal, moderate, with fibrin thrombi, crossbreed domestic pig, porcine.
Conference Note: Salmonella are members of the family Enterobacteriaceae and are primarily associated with self-limiting enteric disease, although they cause systemic, life-threatening illness in some cases. The organisms are non-sporulating, Gram-negative, bacilli which measure 2-5mm in length and 0.7-1.5mm in width. The bacteria move by means of peritrichous flagella. Currently, the various salmonellae are classified as a single species known as Salmonella enterica. Many serovars of S. enterica are known to exist, and substitution of the serovar name for the species is common. The classic form of salmonellosis in humans is known as typhoid fever and is caused by S. typhi. Some species of Salmonella are host specific, such as S. typhi in humans and S. cholerasuis in swine. Other species (serovars) of the genus, such as S. typhimurium, infect a wide range of animals causing gastroenteritis, occasionally leading to septicemia. The disease is most frequent in cattle, horses, and swine, and is uncommon in dogs and cats. Reptiles may be subclinical carriers of the organism and serve as a source of zoonotic infection to humans.
Infection is acquired by ingestion of bacteria. Bacteria that survive passage through the stomach invade intestinal epithelial cells at villar tips. Invasion genes induced by low oxygen tension in the intestine control entrance of bacteria into enterocytes. These genes encode proteins associated with adhesion of the organism and recruitment of host cell cytoskeletal proteins, causing internalization of the bacterium. Invasion of the mucosa, injury to enterocytes, host inflammatory response, and sloughing of enterocytes cause gastroenteritis and diarrhea. Some salmonella may elaborate heat-labile enterotoxins that increase adenyl cyclase in enterocytes and stimulate secretion of fluid by the intestinal mucosa, exacerbating diarrhea and fluid loss. After penetrating the epithelium, the bacteria enter the lamina propria and proliferate within the interstitium and within tissue macrophages.
Enteric infection is followed by clinical resolution in most cases, but occasionally bacteremia and endotoxemia develop, especially in young animals. Septicemia occurs when bacteria are transported by macrophages to the mesenteric lymph nodes. The bacteria may spread to many tissues, including joints, spleen, liver, brain, and meninges. Endotoxemia results from the lipopolysaccharide in bacterial cell walls. Lipopolysaccharide induces vascular dilatation, pooling and activation of platelets and leukocytes, hypoglycemia, complement activation, and release of vasoactive amines. Disseminated intravascular coagulation is a common sequela to endotoxemia. Abortions and stillbirths may occur as a result of acute enteritis or septicemia in infected pregnant animals. Chronic carriers may develop as a result of persistently infected phagocytic cells in the liver, spleen, and mesenteric lymph nodes. Shedding of bacteria or reactivation of disease may occur during periods of stress, immunosuppression, or due to other systemic infections.
Contributor: Veterinary Diagnostic Center, Fair Street and East Campus Loop, Lincoln, NE 68583-0907.
1. Barker IK, Van Dreumel AA, Palmer N: The alimentary system. In: Pathology of Domestic Animals, Jubb KVF, Kennedy PC, Palmer N, eds., 4th ed., vol. 2, pp. 213-221, Academic Press, San Diego, CA, 1993.
2. Wilcock BP, Schwartz KJ: Salmonellosis. In: Diseases of Swine, Leman AD, et al., eds., 7th edition, pp. 570-583, Iowa State University Press, Ames, Iowa, 1992.
3. Lawson GHK, Dow C: Porcine salmonellosis: A study of the field disease. J Comp Path 76:363-371, 1966.
4. Jones TC, Hunt RD, King NW: Diseases caused by bacteria. In: Veterinary Pathology, 6th ed., pp. 453-455, Williams and Wilkins, Baltimore, MD, 1997.
5. Greene CE: Salmonellosis. In: Infectious Diseases of the Dog and Cat, Greene CE, ed., 2nd edition, pp. 235-240, WB Saunders Co., Philadelphia, PA, 1998.
6. Cotran RS, Kumar V, Collins T: Infectious diseases. In: Robbins Pathologic Basis of Disease, 6th ed., pp. 356-357, WB Saunders, Philadelphia, PA, 1999.

Case IV - 98-1045 (AFIP 2641073)

Signalment: Four-year-old, lactating, Holstein cow.
History: Over a six week period, ten cows from the lactating herd died. They were noted down in milk production at one milking and found dead at the next milking. Two other cows, including this cow, survived several days with non-specific clinical signs and were euthanatized. This cow had decreased milk production and weight loss.
Gross Pathology: Necropsy findings included generalized lymphadenopathy, enlarged kidneys with radial white streaking in the cortex, white streaks in the heart, and enlarged adrenal glands with obliteration of the architecture. The liver had focal areas of fibrosis centered around portal vessels.
Laboratory Results: Anemia, lymphocytosis, thrombocytopenia, azotemia, elevated creatinine, hypocalcemia, and hyperphosphatemia were present.
Contributor's Diagnoses and Comments: Lymphogranulomatous myocarditis, splenitis, hepatitis, and interstitial nephritis.
Liver, spleen, heart, and kidneys had lymphocytic to lymphogranulomatous inflammation which destroyed much of the parenchyma in those organs. The adrenal glands were obliterated by the inflammation. Eosinophils are numerous in some lesions. The liver also has phlebitis of the portal veins which may not be present in all slides submitted.
The lesions are similar to those seen in hairy vetch toxicity of cattle, and suggest a type 4 hypersensitivity reaction. No vetch was being fed to these animals, but six weeks prior to the first death citrus pulp was added to the diet. There are several reports of similar disease and pathology in cattle associated with the feeding of citrus pulp. In those reports, the kidneys and heart were most often affected, but multiple organs were usually affected. The severity of disease and organs involved were quite variable. Such was the case in this group of cows. A hemorrhagic syndrome affecting serosal surfaces has been reported in some cases, and this was seen in several of the cows of this outbreak. Vasculitis has been reported in some cases with the hemorrhagic syndrome. Vasculitis was seen in this cow and in another animal, but only in the liver, and was not associated with hemorrhage.
Citrus pulp was fed to the lactating and near term cows in this herd, but the lactating cows received twice the amount of citrus pulp. No disease occurred in the near term cows. Citrus pulp contains several plant lectins, and it is suspected that one of these induces a type 4 hypersensitivity reaction that accounts for the inflammatory reaction seen. Citrus pulp is commonly fed to cattle without causing problems, so there must be other factors involved in the initiation of this disease.
Case 17-4. Kidney. Multifocally expanding the interstitium and replacing selected tubules there is a dense infiltrate of lymphocytes, plasma cells and fewer macrophages.
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Case 17-4. Heart, pericardial fat. Expanding the myocardial interstitium and extending into the pericardial fat there are similar infiltrates of lymphocytes, plasma cells, macrophages, fibroblasts, and occasional foreign body giant cells.
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Case 17-4. Spleen. The white pulp is expanded by similar infiltrates of cells rare foreign body and Langhans giant cells.
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Case 17-4. Liver. Hepatic parenchyma is expanded and replaced by high numbers of eosinophils, lymphocytes, macrophages, and fibroblasts.
AFIP Diagnoses:
1. Kidney: Nephritis, interstitial, granulomatous and eosinophilic, multifocal, moderate, Holstein, bovine.
2. Heart: Myocarditis and epicarditis, granulomatous and eosinophilic, multifocal, moderate, with myofiber degeneration, necrosis, and loss, and pericardial steatitis.
3. Spleen: Splenitis, nodular, granulomatous and eosinophilic, multifocal to coalescing, moderate.
4. Liver: Hepatitis, portal and periportal, lymphohistiocytic and eosinophilic, diffuse, moderate, with portal phlebitis and mild biliary hyperplasia.
Note: Numbers of eosinophils and multinucleate giant cells vary within organs and in areas examined. Some sections of heart contain sarcocysts.
Conference Note: A syndrome of pyrexia, dermatitis, and hemorrhage with similarities to hairy vetch toxicity has been reported in dairy cows in several countries, including the United States, England, Wales, France and the Netherlands. Affected animals present with a wide variety of clinical and pathological syndromes, including pruritic and papular eruptions of the head, neck, tailhead, and udder, mononuclear and eosinophilic inflammatory infiltrates with multinucleate giant cells in various organs, and hemorrhage.
The cause of the disease is uncertain, but several etiologies have been proposed including mycotoxin T2, ochratoxin A, citrinin, di-ureido-isobutane (DUIB) feed additive, sweet vernal hay containing dicoumarol, and introduction of new silage to the herd. Despite the uncertainty of the inciting agent(s), most reports describe similar histopathological features that include varying infiltrates of lymphocytes, macrophages, multinucleate giant cells and eosinophils with multifocal granulomas in a variety of organs, including the kidneys, heart, liver, spleen, adrenal glands, and lymph nodes; vasculitis and thromboses are occasionally reported. These microscopic findings seem to represent a common inflammatory response to a variety of related causes. This condition of dairy cows has similar pathological features to idiopathic eosinophilic dermatitis of the horse.
The contributor notes that, in addition to plant lectins, other factors are likely involved in the initiation of disease in dairy cows. In an outbreak of pruritus, pyrexia, and hemorrhagic syndrome of cows in England, clinical signs occurred in some animals within three days of starting a new feed containing citrus pulp, and several within the herd died over a course of one month while on the ration. In this case, the citrus pulp was found to be moldy, and the mycotoxin citrinin was identified in the feed and implicated as the cause of the disease.
Contributor: Department of Biomedical Sciences and Pathobiology, College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061-0442.
1. Griffiths B, Done SH: Citrinin as a possible cause of the pruritus pyrexia, and hemorrhagic syndrome of cattle. Vet Record 129:113-117, 1991.
2. Panciera RJ: Hairy vetch (Vicia villosa roth) poisoning in cattle. In: Effects of Poisonous Plants on Livestock, Keeler RJ, James LF, eds., pp. 555-563, Academic Press, New York, 1978.
3. Yager JA, Scott DW: The skin and appendages. In: Pathology of Domestic Animals, Jubb KVF, Kennedy PC, Palmer N, eds., 4th ed., vol. 1, pp. 591-592, Academic Press, San Diego, CA, 1993.
Ed Stevens, DVM
Captain, United States Army
Registry of Veterinary Pathology*
Department of Veterinary Pathology
Armed Forces Institute of Pathology
(202)782-2615; DSN: 662-2615
* The American Veterinary Medical Association and the American College of Veterinary Pathologists are co-sponsors of the Registry of Veterinary Pathology. The C.L. Davis Foundation also provides substantial support for the Registry.
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